02500nas a2200361 4500000000100000008004100001260001300042653001500055653001000070653001600080653002100096653001100117653002300128653001100151653002000162653001900182653001200201653000900213653001600222100001400238700001400252700001100266700001500277700001200292700001400304700001300318700001400331245006000345300001100405490000700416520170100423022001402124 1983 d c1983 Nov10aAdolescent10aAdult10aAmyloidosis10aErythema Nodosum10aFemale10aGlomerulonephritis10aHumans10aKidney Diseases10aKidney Tubules10aleprosy10aMale10aMiddle Aged1 aChugh K S1 aDamle P B1 aKaur S1 aSharma B K1 aKumar B1 aSakhuja V1 aNath I V1 aDatta B N00aRenal lesions in leprosy amongst north Indian patients. a707-110 v593 a

Sixty consecutive patients with leprosy were investigated for renal involvement. Clinically overt renal disease was present in 4 patients; 3 presented with a nephrotic state and one patient with progressive renal failure. Urinalysis showed daily protein loss ranging from 0.4 to 8.9 g in 8 patients and microscopic haematuria in 4 cases. Elevated levels of blood urea and creatinine were seen only in one patient with diffuse proliferative glomerulonephritis. Of the 36 patients in whom distal tubular functions were evaluated, concentration and/or acidification defects were detected in 9 patients (25%). Renal histology revealed no abnormality in any of these patients. Serum C3 levels were decreased in 5 patients with lepromatous leprosy and 3 patients with borderline leprosy. Histological evidence of renal involvement was detected in 9 patients (15%). Amyloid deposits were seen in 3 (5%) patients of whom 2 had lepromatous leprosy and one had tuberculoid leprosy with chronic trophic ulcers. Mesangial proliferative lesions were seen in 5 (8.3%) and diffuse proliferative lesions (with crescents in more than 70% of glomeruli) in one patient. All of them had lepromatous leprosy. Three of the 5 patients with mesangial proliferative glomerulonephritis had erythema nodosum leprosum at the time of biopsy. Immunofluorescence studies revealed granular deposits of IgA, IgM and C3 in one patient with mesangial proliferation and IgA/IgM with or without C3 in 3 more patients in whom renal histology was normal. Glomerulonephritis associated with leprosy appears to be immune mediated but confirmation requires identification of lepra antigen in the glomerular immune complex deposits.

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